We propose to determine the factors which regulate the intracellular pool sizes of the adenine nucleotides and of inorganic phosphate in ascites tumor cells. We will approach the problem by studying the partial adenine nucleotide degradation promoted by glucose and the extensive degradation promoted by the phosphorylatable but nonglycolyzable sugar, 2-deoxyglucose. We have preliminary results which suggest that in intact cells inorganic phosphate (one of the products of the degradation) controls the activity of adenylate deaminase, the initial enzyme in the pathway of adenine nucleotide degradation. This finding will be further examined by a kinetic study of the effects of inorganic phosphate on adenylate deaminase purified from ascites tumor cells. The kinetic data will be correlated with intact cell experiments in an attempt to determine the control mechanism operating within the intack ascites tumor cell. Energy production and utilization in ascites tumor cells is disrupted by the partial adenine nucleotide degradation promoted by glucose. However, the adenine nucleotide degradation and altered energy metabolism are associated with what appears to be a normal Crabtree effect. This finding indicates that the Crabtree effect may have different mechanisms depending on the intracellular changes. We propose to examine the effects of the products of the adenine nucleotide degradation on ATP production by isolated ascites tumor mitochondria and will correlate the results with the findings in intact cells. This approach will provide a clearer understanding of tumor cell energy metabolism and new insight into the mechanism of the Crabtree effect.